gopubmed logo
 
find other proteinsAll proteins
GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 27 May 2015.

Ataxia telangiectasia mutated homolog

Atm
serine/threonine protein kinase; critical regulator of the cellular DNA damage response [RGD, Feb 2006] (from NCBI)
Top mentioned proteins: p53, CAN, V1a, HAD, p21
Papers on Atm
Dgcr8 and Dicer are essential for sex chromosome integrity in male meiosis.
New
Grimson et al., Ithaca, United States. In J Cell Sci, 01 Jun 2015
RNA sequencing indicates upregulation of Atm in spermatocytes from microRNA-deficient mice, and immunofluorescence imaging demonstrates an increased abundance of activated ATM kinase and mislocalization of phosphoMDC1, an ATM phosphorylation substrate.
HUS1 regulates in vivo responses to genotoxic chemotherapies.
New
Weiss et al., Ithaca, United States. In Oncogene, 27 May 2015
Central to the DDR are the ATM and ATR kinases, which respond primarily to double-strand DNA breaks (DSBs) and replication stress, respectively.
p53 deficiency-induced Smad1 upregulation suppresses tumorigenesis and causes chemoresistance in colorectal cancers.
New
Li et al., Shanghai, China. In J Mol Cell Biol, 30 Apr 2015
Our previous studies have shown that Smad1 is upregulated and activated by Atm in DNA damage response, which can further bind to p53 and promote p53 stabilization.
Tumor cells, but not endothelial cells, mediate eradication of primary sarcomas by stereotactic body radiation therapy.
New
Kirsch et al., Durham, United States. In Sci Transl Med, 11 Apr 2015
We selectively mutated the proapoptotic gene Bax or the DNA damage response gene Atm to genetically manipulate the radiosensitivity of endothelial cells in primary soft tissue sarcomas.
DNA damage primes the type I interferon system via the cytosolic DNA sensor STING to promote anti-microbial innate immunity.
New
Impact
Gekara et al., Umeå, Sweden. In Immunity, Mar 2015
Dysfunction in Ataxia-telangiectasia mutated (ATM), a central component of the DNA repair machinery, results in Ataxia Telangiectasia (AT), a cancer-prone disease with a variety of inflammatory manifestations.
ATM Regulates Adipocyte Differentiation and Contributes to Glucose Homeostasis.
New
Mizutani et al., Tokyo, Japan. In Cell Rep, Mar 2015
We found that Atm(-/-) mice were insulin resistant and possessed less subcutaneous adipose tissue as well as a lower level of serum adiponectin than Atm(+/+) mice.
Anthracyclines induce DNA damage response-mediated protection against severe sepsis.
Impact
Moita et al., Lisbon, Portugal. In Immunity, 2013
This salutary effect is strictly dependent on the activation of DNA damage response and autophagy pathways in the lung, as demonstrated by deletion of the ataxia telangiectasia mutated (Atm) or the autophagy-related protein 7 (Atg7) specifically in this organ.
Expression pattern of ataxia telangiectasia mutated (ATM), p53, Akt, and glycogen synthase kinase-3β in the striatum of rats treated with 3-nitropropionic acid.
GeneRIF
Pelegrí et al., Barcelona, Spain. In J Neurosci Res, 2012
We examined whether cellular expression of ataxia telangiectasia mutated, p53, Akt, and glycogen synthase kinase-3beta, were involved in the striatal neurodegeneration in the brains of rats
Pathological neoangiogenesis depends on oxidative stress regulation by ATM.
Impact
Kubota et al., Tokyo, Japan. In Nat Med, 2012
The ataxia telangiectasia mutated (ATM) kinase, a master regulator of the DNA damage response (DDR), acts as a barrier to cellular senescence and tumorigenesis.
Wip1-dependent regulation of autophagy, obesity, and atherosclerosis.
Impact
Bulavin et al., Singapore, Singapore. In Cell Metab, 2012
Here, we show that Wip1 phosphatase, a known negative regulator of Atm-dependent signaling, plays a major role in controlling fat accumulation and atherosclerosis in mice; specifically, Wip1 deficiency prevents both conditions.
Nuclear accumulation of HDAC4 in ATM deficiency promotes neurodegeneration in ataxia telangiectasia.
Impact
Herrup et al., United States. In Nat Med, 2012
Here we report that ataxia telangiectasia mutated (ATM) deficiency causes nuclear accumulation of histone deacetylase 4 (HDAC4) in neurons and promotes neurodegeneration.
Cytoplasmic ATM protein kinase: an emerging therapeutic target for diabetes, cancer and neuronal degeneration.
Review
Burn et al., Sioux Falls, United States. In Drug Discov Today, 2011
The gene mutated in this disease, Atm (A-T mutated), encodes a serine/threonine protein kinase that has been traditionally considered to be a nuclear protein controlling cell-cycle progression.
Common variants near ATM are associated with glycemic response to metformin in type 2 diabetes.
Impact
GeneRIF
Pearson et al., Dundee, United Kingdom. In Nat Genet, 2011
ATM, a gene known to be involved in DNA repair and cell cycle control, plays a role in the effect of metformin upstream of AMP-activated protein kinase, and variation in this gene alters glycemic response to metformin
Mdm2 links genotoxic stress and metabolism to p53.
Review
Li et al., Shanghai, China. In Protein Cell, 2010
Mdm2's oncogenic activity is mainly mediated by p53, which is activated by various stresses, especially genotoxic stress, via Atm (ataxia telangiectasia mutated) and Atr (Atm and Rad3-related).
p53 control of bone remodeling.
Review
Li et al., Shanghai, China. In J Cell Biochem, 2010
Moreover, Atm, c-Abl, and Mdm2, upstream regulators of p53 in DNA damage response, regulate osteoblast differentiation and bone remodeling as well.
ATM is involved in cell-cycle control through the regulation of retinoblastoma protein phosphorylation.
GeneRIF
Camins et al., Barcelona, Spain. In J Cell Biochem, 2010
These data demonstrate how a new molecular network on ATM regulates the cell cycle through the control of pRb phosphorylation.
Myc is required for activation of the ATM-dependent checkpoints in response to DNA damage.
GeneRIF
Frisan et al., Stockholm, Sweden. In Plos One, 2009
data demonstrate that MYC contributes to the activation of the ATM-dependent checkpoint responses, leading to cell death in response to specific genotoxic stimuli
The ataxia protein sacsin is a functional co-chaperone that protects against polyglutamine-expanded ataxin-1.
GeneRIF
Chapple et al., London, United Kingdom. In Hum Mol Genet, 2009
Sacsin knockdown resulted in a reduction in cells expressing polyglutamine-expanded ataxin.
Rad3 and Sty1 function in Schizosaccharomyces pombe: an integrated response to DNA damage and environmental stress?
Review
Sunnerhagen et al., Göteborg, Sweden. In Mol Microbiol, 2008
In Schizosaccharomyces pombe, the Ataxia Telangiectasia-mutated (Atm)/Atm and Rad 3 Related (Atr) homologue Rad3 is an essential regulator of the response to DNA damage and stalled replication forks.
ATM activation and DNA damage response.
Review
Kozlov et al., Brisbane, Australia. In Cell Cycle, 2007
Well before the gene (ATM) mutated in the human genetic disorder ataxia-telangiectasia (A-T) was described it was evident from the clinical, molecular and cellular phenotype of A-T that this gene would play a central role in the DNA damage response.
share on facebooktweetadd +1mail to friends